NFAT2 regulates COX-2 expression and modulates the integrin repertoire in endothelial cells at the crossroads of angiogenesis and inflammation

Mena, Mari-Pau; Papiewska-Pająk, Izabela; Przygodzka, Patrycja; Kozaczuk, Anna; Boncela, Joanna; Cierniewski, Czesław S.

doi:10.1016/j.yexcr.2014.03.008

Cited by 15 publications

(9 citation statements)

References 51 publications

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“…CsA, widely used pharmacological inhibitor, are known to block the calcineurin/NFATc1 signaling pathway 39) . Our results are in agreement with Mena et al 40) , who reported that COX-2 upregulation was inhibited by the NFAT antagonist CsA in endothelial cells.…”

Section: Discussionsupporting

confidence: 94%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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Although nuclear factor of activated T cell (NFAT) plays a key role in inflammation, its anti-inflammatory effects and mechanism of action in periodontitis are still unknown. This study aimed to identify the effects of NFAT on the proinflammatory mediators activated by lipopolysaccharide (LPS) plus nicotine stimulation in human periodontal ligament cells (hPDLCs). The production of nitric oxide (NO) and prostaglandin E2 (PGE2) was evaluated using Griess reagent and an enzyme immunoassay, respectively. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and NFAT proteins was evaluated by Western blot analysis. LPS plus nicotine synergistically induced the production of NO and PGE2 and increased the protein expression of iNOS, COX-2 and NFAT. Treatment with an NFAT inhibitor blocked the LPS plus nicotine-stimulated NO and PGE2 release as well as the expression of iNOS and COX-2. Our data suggest that the LPS plus nicotine-induced inflammatory effects on hPDLCs may act through a novel mechanism involving the action of NFAT. Thus, NFAT may provide a potential therapeutic target for the treatment of periodontal disease associated with smoking and dental plaque.

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Section: Discussionsupporting

confidence: 94%

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Lee¹,

Yu²

2015

Journal of dental hygiene science

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“…However, growth factors also regulate the synthesis of specific integrins. Mena et al observed that stimulating human umbilical vein endothelial cells (HUVECs) with VEGF-A increased the production of alpha5 and beta1 integrin subunits (232). Similarly, our research group has shown that a peptide derived from the knuckle epitope of BMP-9 increased the amount of alphav integrin subunits in the plasma membrane of MC3T3-E1 preosteoblasts attached to PS coated with peptides derived from BSP (233).…”

Section: Influence Of Ecm-integrin Interactions On Cell Behaviorsupporting

confidence: 55%

Interactions between bone cells and biomaterials An update

et al. 2016

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As the populations of the Western world become older, they will suffer more and more from bone defects related to osteoporosis (non-union fractures, vertebral damages), cancers (malignant osteolysis) and infections (osteomyelitis). Autografts are usually used to fill these defects, but they have several drawbacks such as morbidity at the donor site and the amount and quality of bone that can be harvested. Recent scientific milestones made in biomaterials development were shown to be promising to overcome these limitations. Cell interactions with biomaterials can be improved by adding at their surface functional groups such as adhesive peptides and/or growth factors. The development of such biomimetic materials able to control bone cell responses can only proceed if it is based on a sound understanding of bone cell behavior and regulation. This review focuses on bone physiology and the regulation of bone cell differentiation and function, and how the latest advances in biomimetic materials can be translated within promising clinical outcomes.

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“…Genistein was demonstrated to significantly inhibit cell apoptosis via downregulation of the PI3K/AKT and HIF-1α signaling pathways. Furthermore, due to the importance of the NF-κB and COX-2 signaling pathways in apoptosis (32,33), the present study hypothesized that genistein may inhibit these pathways in A549 cells and antagonize apoptosis. These results revealed that genistein significantly inhibited apoptosis via suppressing the NF-κB and COX-2 signaling pathways in lung cancer cells.…”

Section: Discussionmentioning

confidence: 90%

Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF-1α/VEGF and NF-κB/COX-2 signaling pathways

Zhang

Su²,

et al. 2017

Molecular Medicine Reports

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Genistein is an important chemopreventive agent against atherosclerosis and cancer. However, whether genistein is effective in the treatment of lung cancer, and its underlying mechanism, remains to be determined. The present study demonstrated that genistein treatment of A549 lung cancer cells decreased viability in a dose‑ and time‑dependent manner, and induced apoptosis. Additionally, A549 cells exhibited significantly increased reactive oxygen species formation and cytochrome‑c leakage, and activated caspase‑3, B‑cell lymphoma 2‑associated X protein and apoptosis inducing factor expression levels, which are involved in the mitochondrial apoptosis pathway. Furthermore, the phosphatidylinositol‑4,5‑biphosphate 3‑kinase (PI3K)/protein kinase B (AKT)/hypoxia‑inducible factor‑1α (HIF‑1α) and nuclear factor‑κB (NF‑κB)/cyclooxygenase‑2 (COX‑2) signaling pathways were significantly downregulated by genistein treatment. In conclusion, reduced proliferation and increased apoptosis in A549 lung cancer cells was associated with inhibition of the PI3K/AKT/HIF‑1α/ and NF‑κB/COX‑2 signaling pathways, which implicates genistein as a potential chemotherapeutic agent for the treatment of lung cancer.

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NFAT2 regulates COX-2 expression and modulates the integrin repertoire in endothelial cells at the crossroads of angiogenesis and inflammation

Cited by 15 publications

References 51 publications

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

NFATc Mediates Lipopolysaccharide and Nicotine-Induced Expression of iNOS and COX-2 in Human Periodontal Ligament Cells

Interactions between bone cells and biomaterials An update

Genistein decreases A549 cell viability via inhibition of the PI3K/AKT/HIF-1α/VEGF and NF-κB/COX-2 signaling pathways

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